The relationship between maternal alcohol abuse and undesirable outcomes of pregnancy has been recognized since ancient times, but only recently has it gained more scientific validation. Both clinical and animal studies have presented convincing evidence that ethanol has deleterious effects on the developing organism. These deleterious effects range from gross skeletal and/or organ defects to behavioral disturbances and mental insufficiency. In light of the interrelationship between biochemical imbalances and functional defects, it would not be surprising if biochemical alterations are found in these offspring that might ultimately identify the basis of the defect and aid in prognosis and treatment. Based upon the literature and our pilot data, there is reason to suspect that offspring exposed in utero to ethanol may have an atypical hypothalamo-hypophyseal-adrenocortical (HHA) system that may be responsible for some of the behavioral effects observed. We propose to examine three aspects of this system in mice exposed to ethanol at various times during gestation. Specifically, we will examine the ontogeny, periodicity, and responsivity of this system.